Porcine Glucose transporter 2,GLUT2 ELISA Kit
- Known as:
- Porcine Glucose transporter 2,GLUT2 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- BLS0017Po
- Product Quantity:
- 48T
- Category:
- -
- Supplier:
- bester
- Gene target:
- Porcine Glucose transporter 2 GLUT2 ELISA Kit
Related genes to: Porcine Glucose transporter 2,GLUT2 ELISA Kit
- Gene:
- SLC2A2 NIH gene
- Name:
- solute carrier family 2 member 2
- Previous symbol:
- GLUT2
- Synonyms:
- -
- Chromosome:
- 3q26.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-01-13
- Date modifiied:
- 2016-02-17
- Gene:
- SLC17A6 NIH gene
- Name:
- solute carrier family 17 member 6
- Previous symbol:
- -
- Synonyms:
- DNPI, VGLUT2
- Chromosome:
- 11p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-27
- Date modifiied:
- 2016-02-17
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- Proopiomelanocortin (POMC) neurons contribute to the regulation of many physiological processes; the majority of which have been attributed to the release of peptides produced from the POMC prohormone such as α-MSH, which plays key roles in food intake and metabolism. However, it is now clear that POMC neurons also release amino acid transmitters that likely contribute to the overall function of POMC cells. Recent work indicates that constitutive deletion of these transmitters can affect metabolic phenotypes, but also that the expression of GABAergic or glutamatergic markers changes throughout development. The goal of the present study was to determine whether the release of glutamate or GABA from POMC neurons in the adult mouse contributes notably to energy balance regulation. Disturbed release of glutamate or GABA specifically from POMC neurons in adult mice was achieved using a tamoxifen-inducible construct ( expressed in mice also carrying floxed versions of or and , encoding the vesicular glutamate transporter type 2 and GAD67 and GAD65 proteins, respectively. All mice in the experiments received tamoxifen injections, but control mice lacked the tamoxifen-inducible Cre sequence. Body weight was unchanged in and - or -deleted female and male mice. Additionally, no significant differences in glucose tolerance or refeeding after an overnight fast were observed. These data collectively suggest that the release of GABA or glutamate from POMC neurons in adult mice does not significantly contribute to the metabolic parameters tested here. In light of prior work, the data also suggest that amino acid transmitter release from POMC cells may contribute to separate functions in the adult versus the developing mouse. - Source: PubMed
Publication date: 2020/09/16
Rau Andrew RKing Connie MHentges Shane T - Anorexigenic melanocortins decrease food intake by activating MC3/MC4 receptors (MC3/4R); the prevailing view is that the orexigenic neuropeptide agouti-related peptide (AgRP) exerts the opposite action by acting as an antagonist at MC3/MC4 receptors. A total of 370 hypothalamic ventromedial nucleus (VMH) glutamatergic neurons was studied using whole-cell recording in hypothalamic slices from a novel mouse expressing green fluorescent protein (GFP) under control of the vesicular glutamate transporter 2 (vGluT2) promoter. Massive numbers of GFP-expressing VMH dendrites extended out of the core of the nucleus into the surrounding cell-poor shell. VMH dendrites received frequent appositions from AgRP-immunoreactive axons in the shell of the nucleus, but not the core, suggesting that AgRP may influence target VMH neurons. alpha-MSH, melanotan II (MTII), and selective MC3R or MC4R agonists were all inhibitory, reducing the spontaneous firing rate and hyperpolarizing vGluT2 neurons. The MC3/4R antagonist SHU9119 was excitatory. Unexpectedly, AgRP did not attenuate MTII actions on these neurons; instead, these two compounds showed an additive inhibitory effect. In the absence of synaptic activity, no hyperpolarization or change in input resistance was evoked by either MTII or AgRP, suggesting indirect actions. Consistent with this view, MTII increased the frequency of spontaneous and miniature IPSCs. In contrast, the mechanism of AgRP inhibition was dependent on presynaptic inhibition of EPSCs mediated by G(i)/G(o)-proteins, and was attenuated by pertussis toxin and NF023, inconsistent with mediation by G(s)-proteins associated with MC receptors. Together, our data suggest that the mechanism of AgRP actions on these excitatory VMH cells appears to be independent of the actions of melanocortins on MC receptors. - Source: PubMed
Fu Li-Yingvan den Pol Anthony N